The vasopressin‐induced excitation of hypoglossal and facial motoneurons in young rats is mediated by V1a but not V1b receptors, and is independent of intracellular calcium signalling

Abstract

As a hormone, vasopressin binds to three distinct receptors: V1a and V1b receptors, which induce phospholipase-Cbeta (PLCbeta) activation and Ca2+ mobilization; and V2 receptors, which are coupled to adenylyl cyclase. V1a and V1b receptors are also present in neurons. In particular, hypoglossal (XII) and facial (VII) motoneurons are excited following vasopressin-V1a receptor binding. The aim of the present study was double: (i) to determine whether V1b receptors contribute to the excitatory effect of vasopressin in XII and VII motoneurons; and (ii) to establish whether the action of vasopressin on motoneurons is mediated by Ca2+ signalling. Patch-clamp recordings were performed in brainstem slices of young rats. Vasopressin depolarized the membrane or generated an inward current. By contrast, [1-deamino-4-cyclohexylalanine] arginine vasopressin (d[Cha4]AVP), a V1b agonist, had no effect. The action of vasopressin was suppressed by Phaa-D-Tyr(Et)-Phe-Gln-Asn-Lys-Pro-Arg-NH2, a V1a antagonist, but not by SSR149415, a V1b antagonist. Thus, the vasopressin-induced excitation of brainstem motoneurons was exclusively mediated by V1a receptors. Light microscopic autoradiography failed to detect V1b binding sites in the facial nucleus. In motoneurons loaded with GTP-gamma-S, a non-hydrolysable analogue of GTP, the effect of vasopressin was suppressed, indicating that neuronal V1a receptors are G-protein-coupled. Intracellular Ca2+ chelation suppressed a Ca2+-activated potassium current, but did not affect the vasopressin-evoked current. H7 and GF109203, inhibitors of protein kinase C, were without effect on the vasopressin-induced excitation. U73122 and D609, PLCbeta inhibitors, were also without effect. Thus, excitation of brainstem motoneurons by V1a receptor activation is probably mediated by a second messenger distinct from that associated with peripheral V1a receptors.

Vasopressin receptors V1aand V2 are not osmosensors

“…However, V1 a R-dependent excitation of motoneurons in a Ca 2+ -, PLC β -, and PKC-independent manner has been demonstrated (Reymond-Marron et al. 2006 ) and the observed V1 a R-dependent cAMP production was proposed to originate from G s activation (Wrobel et al. 2011 ).…”

Mechanism of action of a diterpene alkaloid hypaconitine on cytotoxicity and inhibitory effect of BAPTA‐AM in HCN‐2 neuronal cells

“…This experiment was conducted to explore the pathway of hypaconitine‐induced Ca 2+ entry. The store‐operated Ca 2+ channel modulators ([2‐APB, 50 μM] and [SKF96365, 5 μmol/L]) 21,22 or the PKC inhibitor (GF109203X, 2 μmol/L) 23 was applied 1 minute before 40 μmol/L hypaconitine in Ca 2+ ‐containing medium. Addition of 2‐APB, SKF96365, or GF109203X alone did not alter baseline [Ca 2+ ] i (not shown).…”

Vasopressin facilitates GABAergic transmission in rat hippocampus via activation of V1A receptors

“…AVP has been shown to activate cationic channels (Bisetti et al, 2006; Raggenbass et al, 1991; Reymond-Marron et al, 2006; Wrobel et al, 2011). However, the following results do not support a role of cationic channels in AVP-mediated modulation of GABA release.…”